Fatty15

Masters of Spin

John | The John & Calvin Podcast

Fatty15

C15:0 is emerging as the first essential fatty acid to be discovered in over 90 years.

100+ peer-reviewed studies have been published by independent scientists throughout the world on the benefits of C15:0, including the pure C15:0 ingredient in fatty15.

C15:0 is a pleiotropic nutrient with multiple dose-dependent mechanisms of action.

“#1 fastest-growing supplement company and the 5th fastest-growing Consumer Product Company in America on the Inc. 5000 list”

“Evidence of a nutritional C15:0 deficiency - that’s fixable.”

“Cellular Fragility Syndrome” coined by founder.

Cellular Fragility Syndrome = not having enough C15:0 = fix it with fatty15. - with fatty15.

GRAS

FAQ: “Is it safe to take when pregnant?”

Our ingredient is officially GRAS (generally regarded as safe) certified, which means fatty15 is safe for pregnant women and nursing moms.

In our commitment to make fatty15/FA15/C15:0 accessible to all, we have gone above and beyond to enforce the safety of fatty15 for those of all ages and life stages by receiving GRAS (Generally Recognized As Safe) status by the FDA.

No official “GRAS certification” from the FDA. “Certified” implies FDA approval.

Two Ways to Achieve GRAS Status
- GRAS Notification program: Submit to FDA detailing ingredient. FDA evaluates. GRAS Database
- Self-affirmation: company itself assesses safety of an ingredient and declares it GRAS, without submitting anything to the FDA

“With a recent self-GRAS (Generally Recognized as Safe) affirmation” FA15 can now be used in food and beverage products.
“FA15™ has been approved as a food ingredient that can be used daily, up to 245 mg per day.”

No Public record of evidence used to self-affirm GRAS status.

Fatty15: 3x better than omega-3

Deep Dive: Fatty15 vs. Omega-3

“Simply put, fatty15 is better, broader and safer than the purest, highest performing omega-3 (EPA) in repairing and restoring cellular (aka your) health.”

“Fatty15 repairs 2.5x more cell types compared to omega-3.”

“Fatty15 had 36+ cellular benefits across 83% of cell types tested, which was 3x better than omega-3.”

100% in vitro (cell-based) study, done by founder, unclear if relevant in humans.
3x better?
- 12 vs 36? “36 annotated activities” vs “12 activities shared”?
- but that’s shared, EPA had more. (21, but not reported, must go to supplement)
2.5x more?
- “At 50 μM, EPA was cytotoxic to the following four of the 12 primary human cell systems:”
- “C15:0…36 activities in 10 of the 12 systems in the BioMAP Diversity PLUS Panel”
- Fatty15 repaired 10/12 cell-based systems; omega-3 4/12; 10 / 4 ? therefore 2.5x ?
- Not comparable metrics. That’s mixing different denominators.

Fatty15 instead of omega-3 / EPA

Note: This is a scientific/consumer-protection opinion, not legal advice or an allegation of unlawful conduct.

Unsupported substitution claim. There are no independent, human or animal randomized trials showing C15:0 is superior to EPA/DHA on clinical outcomes; the “3×” claim comes from a single company-affiliated in-vitro screen rather than outcome trials.
Sources: fatty15 “3×” marketing, PLOS ONE in-vitro paper + competing-interest statement
Explicit replacement messaging. The company’s own FAQ says you “may opt to use fatty15 in lieu of omega-3 fish oil supplements.”
Source: fatty15 FAQ
Conflicts with medical consensus. Major authorities advise obtaining EPA/DHA because ALA conversion is limited and fish intake (or Rx EPA) lowers risk in specific populations; telling consumers to replace omega-3s runs counter to that guidance.
Sources: NIH ODS Omega-3 fact sheet, AHA fish/EPA-DHA guidance
Potential for consumer harm. Substitution could dissuade people—especially higher-risk patients—from nutrient and therapies with outcome data (e.g., icosapent ethyl reduces CV events when added to statins).
Sources: NEJM REDUCE-IT trial, FDA label for icosapent ethyl
Likely inadequate substantiation for a comparative health claim. Under FTC standards, comparative efficacy claims require “competent and reliable scientific evidence”—typically well-controlled human studies. An in-vitro screen doesn’t meet that bar.
Source: FTC Health Products Compliance Guidance
Conflicts of interest / non-independence. The in-vitro “3×” paper is authored by company-affiliated inventors with licensed patents; it is not independent and has not been replicated in clinical trials.
Source: PLOS ONE competing-interest statement
Over-extrapolation from cell assays. Cell-panel biomarker differences ≠ clinical benefits in people; dose/exposure relevance and translation are unproven for the claimed endpoints.
Source: PLOS ONE methods/limitations
In my view: borderline unethical. Promoting replacement of EPA/DHA with C15:0 without independent, head-to-head human evidence and against consensus nutrition guidance risks misleading consumers about proven omega-3 benefits.

The analysis above reflects my opinions based on the publicly cited sources and the state of evidence as of September 11, 2025. It is offered for informational and public-interest commentary only. It is not medical or legal advice, and it is not a statement of fact about any company’s intent, ethics, or lawfulness. I do not allege wrongdoing and welcome corrections or additional independent evidence. I have no financial relationship with the products or companies discussed. All trademarks are the property of their respective owners.

Is there any human RCT evidence anyway on fatty15???

Fatty15 and RCTs

Is Fatty15 Legit

“Is Fatty15 Legit” Series: Are there clinical trials supporting C15:0 & fatty15 benefits?

“If you’re here, chances are that you recently heard about fatty15, a healthy aging supplement containing C15:0. And you may be wanting to know if this supplement is legit.”

“Are there clinical trials supporting C15:0 & fatty15 benefits?”

“Yes, there are a growing number of clinical trials supporting C15:0 and fatty15’s health benefits.
Here’s a breakdown of the six clinical trials and seven studies to date:”

Clinical Trial 1

“Stallings et al. led a clinical trial with healthy humans to determine the oral bioavailability and pharmacokinetics of pure C15:0, the same ingredient provided in fatty15.”

“Participants were provided a single oral dose of C15:0 and showed that circulating C15:0 levels reliably increased.
For every 100 mg of ingested pure free fatty acid C15:0, C15:0 circulating levels increased on average by 1 ug/ml.”

Not true.

“Objective: A Malabsorption Blood Test (MBT) is proposed as an alternative method to the 72-hour stool and dietary collection for assessing the degree of fat malabsoption in peaple with pancreatic insufficiency.”

The purpose was to evaluate whether the MBT could detect fat malabsorption in healthy subjects (using Orlistat to inhibit pancreatic lipase) and in cystic fibrosis patients with pancreatic insufficiency.

Not true. This was not a C15:0 dose-response/bioavailability study. They gave participants one 2.5 gram dose (very high) of C15. Nothing about dose response.

“The MBT consists of a simultaneous oral dose of pentadecanoic acid (PA)… and triheptadecanoic acid (THA)… The aim of this study is to demonstrate the ability of MBT to detect fat malabsorption …”

“Materials and methods: The MBT with the PA and THA were delivered in a breakfast test meal (2.5 g PA and either 5g or 8 g THA)”

Clinical Trial 2

“Mascarenhas et al. then led a clinical trial…to extensively model the oral bioavailability and pharmacokinetics of pure C15:0”

“…repeated findings from the Stallings et al. study. Namely, that
for every 100 mg of ingested pure free fatty acid C15:0, circulating C15:0 levels increased on average by 1 ug/ml.”

“The authors concluded that pure free fatty acid C15:0 is, on average, 100% bioavailable.”

Not true. Or at least it is a huge leap from what the study actually did.

Study quote: “The aim of this study was to construct a population model to describe HA and PA pharmacokinetics (PK) after MBT administration.” It’s about validating the MBT.

This is not true. They never modeled this. This is not in the study.

And note:

“Participants consumed the MBT 8-ounce test meal… 2.5 or 5.0 g of PA” (PA is C15:0). 2 dose amounts! GRAMS!

100% bioavailable? What? That is only possible with injection. It is literally ridiculous. 100% bioavailable ON AVERAGE?

Study quote: “The PA bioavailability estimate of 1.07 (95%CI, 0.827, 1.42) for subjects with CF was similar to healthy subjects. The estimate for CF subjects administered enzymes was 0.88 (0.72, 1.09). Although 12.3% lower than in healthy subjects, the 95%CI contains the null value of 1.”

IS that where they got 100%? This is ‘similar’ bioavailability in 2 groups. It says nothing about absolute bioavailability.

Both studies not what they say they are.

Clinical Trial 4

88 Chinese females with NAFLD were randomly assigned to 1 of the 3 groups for 12 wk: diet with C15:0 supplementation (n = 31), diet without C15:0 supplementation (n = 28), or control (habitual diet and no C15:0 supplementation, n = 29). Treatment diet was Asian-adapted Mediterranean diet.

“While all three groups had lowered liver fat and body weight loss, the C15:0 supplemented group trended to having the greatest loss of liver fat and body fat. It is important to note, however, that these shared improvements among all three groups were not statistically significantly between the groups.”

“The authors conclude that C15:0 supplementation had early evidence of providing clinically relevant benefits related to lower LDL cholesterol and an improved gut microbiome.”

Clinical Trial 4

List of Metrics unchanged with addition of C15:

Body weight, BMI, Total fat mass, Fat-free mass, Waist circumference,
Visceral adipose tissue (VAT) volume, Subcutaneous abdominal adipose tissue (SAT) volume, Superficial subcutaneous abdominal adipose tissue (SAT), Deep SAT,

Liver fat (MRI-PDFF), Controlled Attenuation Parameter (CAP) score, Intramyocellular lipid (soleus IMCL/water), Pancreatic fat PDFF (head–body), Pancreatic fat PDFF (tail),

Systolic blood pressure, Diastolic blood pressure, Fasting glucose, Fasting insulin, HOMA-IR, HbA1c, Total cholesterol, HDL-cholesterol, Triglycerides,

Gamma-glutamyl transferase (GGT), Alanine aminotransferase (ALT), Aspartate aminotransferase (AST), Alkaline phosphatase (ALP), C-reactive protein (CRP), Resting metabolic rate (RMR), Physical activity (steps/day),

Sleep duration,
STAI—State anxiety score, STAI—Trait anxiety score, BDI-II depression score,

Gut microbiome: Bacteroides ovatus abundance, Fusobacterium mortiferum abundance

Total Metrics measured: 37
Metrics unchanged with C15: 36
Metrics changed with C15: 1
*it did on average increase C15 levels

Clinical Trial 5

Not a separate clinical trial. Additional data analysis of Trial 4.

“This post-hoc analysis showed that, while all three groups had lower body weight and improved mood, the C15:0 supplemented group had the most significant improvement in mood.

“The authors conclude that C15:0 supplementation may have a positive effect on improving mood.”

Study quotes:

“The present study cannot conclude that the group receiving C+15:0 together with the MD had effects in decreasing symptoms.”
“These findings suggest that both dietary interventions had comparable effects on anxiety and depression within the study population.”

NOT a separate clinical trial.

The original study was NOT set up to test any mental health / anxiety issues.

Not sure why they mention the body weight thing.

Not robust for: “Diet+C15 is better than Diet–C15 or Control on anxiety/depression.” There is no between-arm inferential test to back that. Even the manuscript states it cannot conclude a C15:0 effect on symptoms.

Paired t-tests were employed to assess significant changes over time Only within-group paired t-tests, No between-group modeling of change.

Do the claims live up to the modeling? Not for incremental treatment effects. Paired t-tests address within-arm change, which cannot establish that Diet+C15 outperformed Diet–C15 or Control.

To claim superiority (e.g., “C15:0 improved anxiety beyond diet”), you must test between-arm differences in change (ANCOVA on post-score with baseline covariate, or a mixed model with Group×Time interaction). They didn’t.

Symptoms declined over 12 weeks in this sample across all groups.

Clinical Trial 6

Not on Fatty15 or C15:0 supplementation. It’s on high or moderate dairy fat diets. Much less relevant.

“Clinical Trial 6: Arghavani et al. led a cross-over clinical trial that included healthy adults to evaluate the potential effects of dairy fat diets, as well as individual fatty acid components within dairy fat, on blood pressure and vascular stiffness”. “This clinical trial showed the following:”

The 2025 paper by Arghavani et al. is a secondary analysis of data from an already‐conducted randomized crossover trial.

There is nothing in the original RCT about C15.

Original RCT - “Objective: The aim of this clinical trial was to evaluate the impact of high dairy product intake (HD) (≥4 servings/d) for 6 wk, compared with an adequate dairy product intake (AD) (≤2 servings/d), on glycemic and insulinemic parameters, insulin sensitivity, insulin secretion, and β-cell function in hyperinsulinemic adults.”

Clinical Trial 7

“Kaneko et al. led a randomized, placebo-controlled clinical trial that included older women to evaluate the potential effects of an oral high-C15 algal oil on skin elasticity, collagen density, and skin moisture. This clinical trial showed that daily oral intake of high-C15 algal oil for 12 weeks improved skin elasticity, collagen density, and skin moisture.”

“The authors conclude that oral intake of high C15-containing supplements provides skin health benefits.”

Orlan oil, containing C:15 but also many other fatty acids like DHA, DPA, EPA.
Dose of C15 per day: ~9mg

Summary so far

Of the 6 “clinical trials supporting C15:0 or fatty15 benefits”:

No clinical trial on actual fatty15.
Literal making up of what the study did.
A secondary analysis on an RCT is not an RCT.
C15 doesn’t appear to help NAFLD (even at higher dose that fatty15 recommends)
Almost ZERO evidence it does anything.

Clinical Trial 3

The only RCT in humans on actual on Fatty15.

“Robinson et al. led a randomized, double-blinded and placebo-controlled clinical trial with young adults (ages 18 to 24 years old) at risk of metabolic syndrome and who were purposely avoiding whole fat dairy products”

Among participants who adhered to the protocol, their C15:0 levels increased at the same amounts demonstrated by Mascarenhas et al. and Stallings et al.
Namely, 200 mg of C15:0 resulted in raised circulating C15:0 levels of 2.3 ug/ml.”

C15:0 Plasma Level Increase

“C15:0 levels increased among participants who strictly adhered to the protocol.”

Reverse logic: Groups were formed after the study, based on final C15:0 levels, not on adherence.

below 5 μg/mL -> “sub-threshold”
above 5 μg/mL -> “threshold”

Only half reached the threshold

10 / 20 in the C15:0 arm ended ≥ 5 µg/mL
11 / 30 participants were already ≥ 5 µg/mL at baseline (7/20 in C15:0 arm)

Adherence per group:

95% Threshold group (171 total pills)
84.3% Sub-threshold group (152 total pills)

Change in plasma C15:0 levels from baseline to 12 wk

Half of those on fatty15, taking on average 84.3% of pills (152 total) did not raise C15:0 levels above threshold.

Liver Function in Threshold Group

“Among participants who adhered to the protocol, their C15:0 levels increased…This group with raised C15:0 levels also had significantly improved liver function (lower ALT and AST)”

Subgroup Charts

Kruskal–Wallis

Study Abstract:

“Half of the participants in the treatment group had a posttreatment C15:0 level >5 μg/mL. In these individuals, there were significantly greater decreases in alanine aminotransferase (−29 U/L, P = 0.001) and aspartate aminotransferase (−6 U/L, P = 0.014), as well as a greater increase in hemoglobin (0.60 g/dL, P = 0.010), as compared with participants that did not reach a posttreatment level >5 μg/mL.”

subgroup (threshold) reframed as “particpants who adhered to the protocol”
“significantly improved liver function” and “demonstrating improved red blood cell function” assert clinical efficacy
P values (ALT 0.001; AST 0.014; Hgb 0.010) come from the three-group Kruskal–Wallis test

Three Group Kruskal–Wallis Test

“significantly greater decreases in alanine aminotransferase (−29 U/L, P = 0.001) and aspartate aminotransferase (−6 U/L, P = 0.014), as well as a greater increase in hemoglobin (0.60 g/dL, P = 0.010), as compared with participants that did not reach a posttreatment level >5 μg/mL.”

non-parametric (no distribution assumed)
tells you at least 2 distributions (not just medians) differs from among the 3
not which pairs differ
Medians can mislead—shape matters. KW is based on ranks of all individual values, and it is sensitive to spread and tail behavior
“as compared with participants that did not reach a posttreatment level >5 μg/mL” implies threshold vs (subthreshold + placebo)“. This was not tested.
Small n → unstable medians
KW test does not adjust for baseline differences
sorry, that’s how statistics works.

Clinical Trial 7

List of Metrics unchanged with addition of C15:

Body weight, BMI, Waist circumference, Hip circumference,

Systolic blood pressure, Diastolic blood pressure,

Fasting glucose, Fasting insulin,

Total cholesterol, HDL cholesterol, LDL cholesterol, Triglycerides,

C-reactive protein (CRP), Alanine aminotransferase (ALT), Aspartate aminotransferase (AST), Hemoglobin

Total Metrics measured: 17
Metrics unchanged with fatty15: 16
Metrics changed with fatty15: 1
*it did on average increase C15 levels

fatty15 on the Skeptics

What the skeptics say

In videos, skeptics go over two clinical trials (Robinson et al. and Chooi et al.) and incorrectly conclude that these trials were not in relevant populations and did not demonstrate efficacy.

Strangely, the skeptics made these statements while showing the papers’ abstracts, where the authors themselves concluded that C15:0 demonstrated promising results.

The skeptics do not mention any of the other five studies and four clinical trials provided above, in part because two are recent publications.

HOW MUCH?

but if you still want to try fatty15:

‘30 day’ means 30 pills, means 100mg per pill.
Study protocol of 200mg or 300mg

To recreate the study doses: (based on 90 day subscription)

$2.67 or $4.00 per day, or $80 or $120 per month

What are you paying for? Marketing!

“HSA/FSA eligible”

Fatty15: Another Subscription!

So Many Claims:

“Essential fatty acid” / widespread deficiency
Not supported: C15:0 is not recognized as essential by authorities. Sources: NIH ODS (EFAs = LA & ALA), Company blog
The 3 authors of the study claijmming this are: Founder of fatty15, financed by Epitracker (Venn-Watson owned company), and a scientific advisor to fatty15 who holds equity in the company.
“Cellular Fragility Syndrome”
Not supported: Not a recognized medical diagnosis (absent from ICD-11, not a MeSH descriptor). The term is introduced by company-affiliated authors in a single hypothesis/review and amplified in marketing/press; there is no independent clinical validation or diagnostic criteria. See the hypothesis paper (Venn-Watson 2024), company blog (fatty15), and third-party critique (CSPI).
Metabolic health (PPAR-α/δ, AMPK, mitochondria)
Not supported (human RCTs): 12-wk placebo-controlled trials raised blood C15:0 but no between-group improvements in clinical endpoints except small LDL decrease (1/37), and very very weak “subgroup” analysis for lower AST/ALT.
Sources: J Nutr RCT (2024)
Heart health (LDL; cardiometabolic risk/events)
Neutral/insufficient: No trials show fewer CVD events; observational meta-analysis shows no association with all-cause mortality and non-significant pooled associations for some CVD subtypes for 15:0.
Sources: PLOS Med meta-analysis (2021)
Liver health (enzymes; fatty liver)
Not supported (human): 12 week human RCT trial showed no difference in liver Fat, or liver enzymes (except GGT, (but not in subgroup, lower ALT/AST in subgroup)) Unclear results (placebo increased GGT). Sources: J Nutr RCT, AJCN TANGO RCT (2024)
Red blood cells (membranes; hemoglobin)
Neutral (human ITT): Hemoglobin increase seen only in NON-RANDOM subgroup, not vs placebo in intention-to-treat.
Source: J Nutr RCT
Immune health / inflammation (cytokines, CRP)
Not supported (human): No human RCT showing reductions; both human RCTs showed no difference in CRP in C15 group.
Cognitive & mental health (dopamine/PPAR; mood/stress)
Insufficient (human): No human trials located; claims are marketing. RCT they claim supports this (not RCT, secondary anlaysis of RCT), authors state “The present study cannot conclude that the group receiving C+15:0 together with the MD had effects in decreasing symptoms.” Example claim: Company blog

So Many Claims:

Sleep quality
Insufficient (human): No C15:0 sleep RCTs; “deeper sleep” appears in marketing/surveys. RCT found do difference in sleep duration. Example claim: Product page
Hunger/satiety (PPAR-α)
Insufficient (human): No RCTs measuring appetite/energy intake/GLP-1/ghrelin.
Example claim: Company post
Joint comfort
Insufficient (human): No human RCTs on joint pain/function.
Example claim: Marketing copy
Gut microbiome
Limited/neutral (human): In NAFLD (TABGO) trial, Bifidobacterium adolescentis increase reported with C15:0, but no broader microbiome “health” or clinical GI benefits established.
Source: AJCN TANGO RCT
Anti-aging / “slows and reverses aging”
Not supported (human outcomes): No trials on aging endpoints or epigenetic clocks; mortality association for 15:0 is null in meta-analysis.
Sources: PLOS Med meta-analysis, Homepage claim, “Reversing cellular aging” blog
“Reduces mTOR” (longevity mechanism)
Insufficient (human): Based on mechanistic/cell work, not human outcomes.
Sources: Company mTOR blog, Review asserting AMPK↑/mTOR↓ is written by author and of questionable relevance.
“3× more cellular benefits than EPA (omega-3)” / “take fatty15 instead of omega-3”
Not supported (human); potentially misleading—arguably borderline unethical. The “3×” figure comes incorrect math from a single in-vitro screen by company-affiliated authors; there are NO human RCTs or animal RCTs showing clinical superiority over EPA. Substitution messaging (implying you should take fatty15 instead of omega-3) conflicts with established recommendations that EPA/DHA remain important nutrients. Comparative health claims promoting substitution away from EPA/DHA conflicts with consensus guidance and, without competent and reliable human evidence, should be backed by competent and reliable scientific evidence, typically well-controlled human trials—which is not present here, a concern under FTC health-claims standards.
Sources: Company claim, FTC Health Products Compliance Guidance, NIH ODS: Omega-3, AHA: Fish & omega-3
Note: This is a scientific/consumer-protection opinion, not legal advice or an allegation of unlawful conduct.